Protein Metabolism Research Lab, Department of Kinesiology, McMaster University, Hamilton, ON, Canada; Research Institute for Sport & Exercise Sciences, Liverpool John Moores University, Liverpool, United Kingdom.
Research Institute for Sport & Exercise Sciences, Liverpool John Moores University, Liverpool, United Kingdom.
Free Radic Biol Med. 2024 Oct;223:341-356. doi: 10.1016/j.freeradbiomed.2024.08.010. Epub 2024 Aug 13.
The mechanisms leading to a predominantly hypertrophied phenotype versus a predominantly oxidative phenotype, the hallmarks of resistance training (RT) or aerobic training (AT), respectively, are being unraveled. In humans, exposure of naïve persons to either AT or RT results in their skeletal muscle exhibiting generic 'exercise stress-related' signaling, transcription, and translation responses. However, with increasing engagement in AT or RT, the responses become refined, and the phenotype typically associated with each form of exercise emerges. Here, we review some of the mechanisms underpinning the adaptations of how muscles become, through AT, 'fit' and RT, 'mighty.' Much of our understanding of molecular exercise physiology has arisen from targeted analysis of post-translational modifications and measures of protein synthesis. Phosphorylation of specific residue sites has been a dominant focus, with canonical signaling pathways (AMPK and mTOR) studied extensively in the context of AT and RT, respectively. These alone, along with protein synthesis, have only begun to elucidate key differences in AT and RT signaling. Still, key yet uncharacterized differences exist in signaling and regulation of protein synthesis that drive unique adaptation to AT and RT. Omic studies are required to better understand the divergent relationship between exercise and phenotypic outcomes of training.
导致主要表现为肥大表型或主要表现为氧化表型的机制，分别是抗阻训练（RT）或有氧训练（AT）的标志，正在被揭示。在人类中，将未经训练的人暴露于 AT 或 RT 下，会导致其骨骼肌表现出一般性的“运动应激相关”信号转导、转录和翻译反应。然而，随着 AT 或 RT 的参与度增加，这些反应变得更加精细，与每种运动形式相关的表型通常会显现出来。在这里，我们回顾了一些机制，这些机制支撑着肌肉如何通过 AT 变得“适应”，以及如何通过 RT 变得“强大”。我们对分子运动生理学的理解很大程度上源于对翻译后修饰和蛋白质合成测量的靶向分析。特定残基位点的磷酸化一直是一个主要关注点，经典的信号通路（AMPK 和 mTOR）分别在 AT 和 RT 的背景下进行了广泛研究。这些以及蛋白质合成，仅开始阐明 AT 和 RT 信号转导的关键差异。尽管如此，在信号转导和蛋白质合成的调控方面仍存在关键但尚未确定的差异，这些差异驱动了对 AT 和 RT 的独特适应。需要进行组学研究来更好地理解运动与训练表型结果之间的分歧关系。
